Studies are proposed to test the popular but still unproven hypothesis that sympathetic overactivity contributes importantly to the production of hypertension. Crucial evidence supporting this hypothesis is the demonstration by Folkow and Rubinstein that chronic hypothalamic stimulation increases systolic pressure (measured once a week with a tail-cuff method) in awake rats. But since their results were only preliminary and have never been confirmed, I propose to re-examine the problem by measuring arterial pressure directly from indwelling catheters as well as indirectly with a sensitive tail-cuff method. To allow estimation of changes in cardiac output and peripheral resistance in unanesthetized rats, indwelling electromagnetic flowprobes will be implanted chronically around the ascending aorta. The neurologic mechanisms causing cardiovascular responses to posterior hypothalamic stimulation will be assessed by recording electrical activity in the various afferent and efferent nerves. In addition, the cardiovascular consequences of electrolytic or chemical lesions of the posterior hypothalamus will be studied. Instead of relying on hypothalamic stimulation solely, other experiments will explore the possibility that sustained hypertension results from chronic exposure to a combination of predisposing factors. Because cardiovascular function is normally regulated by the sympathetic nervous system, my working hypothesis assumes that the primary disturbance in hypertension is one of sympathetic overactivity. Based on the known interaction between sympathetic nerves and various organs, induction of hypertension will be attempted by combining continuous electrical stimulation of hypothalamic vasomotor centers with change in salt intake, renal, or adrenocortical function.